We have continued to evaluate the mechanism of the blood pressure response induced by osmotic and nonosmotic stimuli of arginine vasopressin (AVP). To further define the hemodynamics responsible for these changes, a method for the repetitive measurement of cardiac output in awake partially restrained rats was developed. We have proven this technique based on the thermodilution principle to be reliable and reproducible for periods up to 70 hours post catheter placement. The increase in BP noted with hypertonic saline in the Long Evans strain of rats is the result of a significant increase in peripheral resistance with an associated decline in cardiac output. Brattleboro rats had a minimal increase in blood pressure and a 5% increase in cardiac output, with no significant change in peripheral resistance. These findings are consistent with our previously reported results in unrestrained animals. Unrestrained Long Evans and Brattleboro rats increassed mean arterial pressure 31 and 5 mm Hg respectively, while in unrestrained rats the changes were 37and 3 mm Hg respectively.